Comparative investigation of the pathogenicity of three Mycobacterium tuberculosis mutants defective in the synthesis of p-hydroxybenzoic acid derivatives.

Brigitte Gicquel; Ruth Griffin; Michel Huerre; Patricia Constant; Avraham Liav; Iveta Bottova; Jerome Nigou; Therese Brando; Germain Puzo; Mamadou Daffe; Pearline Benjamin; Stephen Coade; Roger S. Buxton; Ricardo E. Tascon; Aaron Rae; Brian D. Robertson; Douglas B. Lowrie; Douglas B. Young; Gustavo Stadthagen; Mary Jackson; Patricia Charles; Frederic Boudou; Nathalie Barilone

doi:10.1016/j.micinf.2006.04.008

Comparative investigation of the pathogenicity of three Mycobacterium tuberculosis mutants defective in the synthesis of p-hydroxybenzoic acid derivatives.

Brigitte Gicquel, Ruth Griffin, Michel Huerre, Patricia Constant, Avraham Liav, Iveta Bottova, Jerome Nigou, Therese Brando, Germain Puzo, Mamadou Daffe, Pearline Benjamin, Stephen Coade, Roger S. Buxton, Ricardo E. Tascon, Aaron Rae, Brian D. Robertson, Douglas B. Lowrie, Douglas B. Young, Gustavo Stadthagen, Mary JacksonPatricia Charles, Frederic Boudou, Nathalie Barilone

Research output: Contribution to journal › Article › peer-review

Abstract

p-Hydroxybenzoic acid derivatives (p-HBADs) are glycoconjugates secreted by all Mycobacterium tuberculosis isolates whose contribution to pathogenicity remains to be determined. The pathogenicity of three transposon mutants of M. tuberculosis deficient in the biosynthesis of some or all forms of p-HBADs was studied. Whilst the mutants grew similarly to the wild-type strain in macrophages and C57BL/6 mice, two of the mutants induced a more severe and diffuse inflammation in the lungs. The lack of production of some or all forms of p-HBADs in these two mutants also correlated with an increased secretion of the pro-inflammatory cytokines tumour-necrosis factor α, interleukin 6 and interleukin 12 in vivo. We propose that the loss of production of p-HBADs by tubercle bacilli results in their diminished ability to suppress the pro-inflammatory response to infection and that this ultimately provokes extensive pulmonary lesions in the C57BL/6 model of tuberculosis infection.

Original language	English
Pages (from-to)	2245-2253
Journal	Microbes and Infection
Volume	8
Issue number	8
DOIs	https://doi.org/10.1016/j.micinf.2006.04.008
Publication status	Published - Jul 2006
Externally published	Yes

Bibliographical note

Note: This work was supported by the European Commission, within the 5th and 6th Framework contract numbers; QLK2-CT-1999-01093 and LSHP-CT-2003-503367, the CONACyT fellowship no. 175523 from Mexico, the National Institutes of Health grant RO1 AI064798-01, the Marie Curie Training Site program no. CT-2000-00058 from the European Commission, the Medical Research Council and the Wellcome Trust and the Burroughs Wellcome Foundation, reference number 059125/Z/99/A.

Keywords

Biological sciences

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Griffin-R-33833-AAMAccepted author manuscript, 1.46 MBLicence: CC BY-NC-ND

http://doi.org/10.1016/j.micinf.2006.04.008

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Gicquel, B., Griffin, R., Huerre, M., Constant, P., Liav, A., Bottova, I., Nigou, J., Brando, T., Puzo, G., Daffe, M., Benjamin, P., Coade, S., Buxton, R. S., Tascon, R. E., Rae, A., Robertson, B. D., Lowrie, D. B., Young, D. B., Stadthagen, G., ... Barilone, N. (2006). Comparative investigation of the pathogenicity of three Mycobacterium tuberculosis mutants defective in the synthesis of p-hydroxybenzoic acid derivatives. Microbes and Infection, 8(8), 2245-2253. https://doi.org/10.1016/j.micinf.2006.04.008

@article{3119e684eb4148f09d7d08d04d468151,

title = "Comparative investigation of the pathogenicity of three Mycobacterium tuberculosis mutants defective in the synthesis of p-hydroxybenzoic acid derivatives.",

abstract = "p-Hydroxybenzoic acid derivatives (p-HBADs) are glycoconjugates secreted by all Mycobacterium tuberculosis isolates whose contribution to pathogenicity remains to be determined. The pathogenicity of three transposon mutants of M. tuberculosis deficient in the biosynthesis of some or all forms of p-HBADs was studied. Whilst the mutants grew similarly to the wild-type strain in macrophages and C57BL/6 mice, two of the mutants induced a more severe and diffuse inflammation in the lungs. The lack of production of some or all forms of p-HBADs in these two mutants also correlated with an increased secretion of the pro-inflammatory cytokines tumour-necrosis factor α, interleukin 6 and interleukin 12 in vivo. We propose that the loss of production of p-HBADs by tubercle bacilli results in their diminished ability to suppress the pro-inflammatory response to infection and that this ultimately provokes extensive pulmonary lesions in the C57BL/6 model of tuberculosis infection.",

keywords = "Biological sciences",

author = "Brigitte Gicquel and Ruth Griffin and Michel Huerre and Patricia Constant and Avraham Liav and Iveta Bottova and Jerome Nigou and Therese Brando and Germain Puzo and Mamadou Daffe and Pearline Benjamin and Stephen Coade and Buxton, \{Roger S.\} and Tascon, \{Ricardo E.\} and Aaron Rae and Robertson, \{Brian D.\} and Lowrie, \{Douglas B.\} and Young, \{Douglas B.\} and Gustavo Stadthagen and Mary Jackson and Patricia Charles and Frederic Boudou and Nathalie Barilone",

note = "Note: This work was supported by the European Commission, within the 5th and 6th Framework contract numbers; QLK2-CT-1999-01093 and LSHP-CT-2003-503367, the CONACyT fellowship no. 175523 from Mexico, the National Institutes of Health grant RO1 AI064798-01, the Marie Curie Training Site program no. CT-2000-00058 from the European Commission, the Medical Research Council and the Wellcome Trust and the Burroughs Wellcome Foundation, reference number 059125/Z/99/A.",

year = "2006",

month = jul,

doi = "10.1016/j.micinf.2006.04.008",

language = "English",

volume = "8",

pages = "2245--2253",

journal = "Microbes and Infection",

issn = "1286-4579",

publisher = "Elsevier Masson s.r.l.",

number = "8",

}

Gicquel, B, Griffin, R, Huerre, M, Constant, P, Liav, A, Bottova, I, Nigou, J, Brando, T, Puzo, G, Daffe, M, Benjamin, P, Coade, S, Buxton, RS, Tascon, RE, Rae, A, Robertson, BD, Lowrie, DB, Young, DB, Stadthagen, G, Jackson, M, Charles, P, Boudou, F & Barilone, N 2006, 'Comparative investigation of the pathogenicity of three Mycobacterium tuberculosis mutants defective in the synthesis of p-hydroxybenzoic acid derivatives.', Microbes and Infection, vol. 8, no. 8, pp. 2245-2253. https://doi.org/10.1016/j.micinf.2006.04.008

TY - JOUR

T1 - Comparative investigation of the pathogenicity of three Mycobacterium tuberculosis mutants defective in the synthesis of p-hydroxybenzoic acid derivatives.

AU - Gicquel, Brigitte

AU - Griffin, Ruth

AU - Huerre, Michel

AU - Constant, Patricia

AU - Liav, Avraham

AU - Bottova, Iveta

AU - Nigou, Jerome

AU - Brando, Therese

AU - Puzo, Germain

AU - Daffe, Mamadou

AU - Benjamin, Pearline

AU - Coade, Stephen

AU - Buxton, Roger S.

AU - Tascon, Ricardo E.

AU - Rae, Aaron

AU - Robertson, Brian D.

AU - Lowrie, Douglas B.

AU - Young, Douglas B.

AU - Stadthagen, Gustavo

AU - Jackson, Mary

AU - Charles, Patricia

AU - Boudou, Frederic

AU - Barilone, Nathalie

N1 - Note: This work was supported by the European Commission, within the 5th and 6th Framework contract numbers; QLK2-CT-1999-01093 and LSHP-CT-2003-503367, the CONACyT fellowship no. 175523 from Mexico, the National Institutes of Health grant RO1 AI064798-01, the Marie Curie Training Site program no. CT-2000-00058 from the European Commission, the Medical Research Council and the Wellcome Trust and the Burroughs Wellcome Foundation, reference number 059125/Z/99/A.

PY - 2006/7

Y1 - 2006/7

N2 - p-Hydroxybenzoic acid derivatives (p-HBADs) are glycoconjugates secreted by all Mycobacterium tuberculosis isolates whose contribution to pathogenicity remains to be determined. The pathogenicity of three transposon mutants of M. tuberculosis deficient in the biosynthesis of some or all forms of p-HBADs was studied. Whilst the mutants grew similarly to the wild-type strain in macrophages and C57BL/6 mice, two of the mutants induced a more severe and diffuse inflammation in the lungs. The lack of production of some or all forms of p-HBADs in these two mutants also correlated with an increased secretion of the pro-inflammatory cytokines tumour-necrosis factor α, interleukin 6 and interleukin 12 in vivo. We propose that the loss of production of p-HBADs by tubercle bacilli results in their diminished ability to suppress the pro-inflammatory response to infection and that this ultimately provokes extensive pulmonary lesions in the C57BL/6 model of tuberculosis infection.

AB - p-Hydroxybenzoic acid derivatives (p-HBADs) are glycoconjugates secreted by all Mycobacterium tuberculosis isolates whose contribution to pathogenicity remains to be determined. The pathogenicity of three transposon mutants of M. tuberculosis deficient in the biosynthesis of some or all forms of p-HBADs was studied. Whilst the mutants grew similarly to the wild-type strain in macrophages and C57BL/6 mice, two of the mutants induced a more severe and diffuse inflammation in the lungs. The lack of production of some or all forms of p-HBADs in these two mutants also correlated with an increased secretion of the pro-inflammatory cytokines tumour-necrosis factor α, interleukin 6 and interleukin 12 in vivo. We propose that the loss of production of p-HBADs by tubercle bacilli results in their diminished ability to suppress the pro-inflammatory response to infection and that this ultimately provokes extensive pulmonary lesions in the C57BL/6 model of tuberculosis infection.

KW - Biological sciences

UR - https://www.ncbi.nlm.nih.gov/pubmed/16782391

U2 - 10.1016/j.micinf.2006.04.008

DO - 10.1016/j.micinf.2006.04.008

M3 - Article

C2 - 16782391

SN - 1286-4579

VL - 8

SP - 2245

EP - 2253

JO - Microbes and Infection

JF - Microbes and Infection

IS - 8

ER -

Comparative investigation of the pathogenicity of three Mycobacterium tuberculosis mutants defective in the synthesis of p-hydroxybenzoic acid derivatives.

Abstract

Bibliographical note

Keywords

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